Camillo Tancredi Strizzi
@CTStrizzi
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MD, Nephrology Resident at @policlinicogemelli Currently Research Fellow at Karolinska Institutet Science & Research Enthusiast, Part-time Musician.
Joined October 2023
🧵1. Aldosterone isn’t just “salt & water.” In modern sodium-rich contexts it drives inflammation, fibrosis, and residual cardiorenal risk. We map physiology → disease → therapies, and argue for reprogramming the signal. Follow the thread --->
mdpi.com
Aldosterone is a key regulator of sodium reabsorption, potassium secretion, and acid–base balance along the aldosterone-sensitive distal nephron (ASDN), where it exerts coordinated, segment-specific...
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Now open access in @NDTsocial CKD of unexplained cause (CKDx): A consensus statement by the Genes &Kidney Working Group of the ERA 🧐Check also our 2 open access editorials on this innovative concept. ▶️ https://t.co/E3AlNE29wO
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Full paper available in open access, in collaboration with @Violadmb & @FrancescoPesce. @IJMS_MDPI
https://t.co/Lgow4rVRAh
mdpi.com
Aldosterone is a key regulator of sodium reabsorption, potassium secretion, and acid–base balance along the aldosterone-sensitive distal nephron (ASDN), where it exerts coordinated, segment-specific...
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3. Connecting Tubule/Collecting Duct α-Intercalated cell 🎯 Aldo → H⁺ secretion (H-ATPase/H/K-ATPase) β-Intercalated cell (base/Cl⁻) 🛑Aldo suppresses Pendrin (Cl/HCO₃ handling) 🧪Aldosterone excess contribute to metabolic alkalosis with hypokalemia.
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2. Connecting Tubule/Cortical Collecting Duct Principal cell, ENaC reabsorb Na. 🎯Aldo → ENaC & Na/K-ATPase boost 🎯Aldo → ROMK & BK channel activity for K+ secretion 👉Na⁺ in, K⁺ out.
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1. Distal Convoluted Tubule (thiazide site) Electroneutral NCC reabsorbs NaCl. 🎯Ang II → NCC activity via the WNK-SPAK/OSR1 kinase independently from Aldo 🎯Aldo → NCC protein abundance 🛑high K⁺ inhibits NCC 🤓This is how the kidney can retain Na⁺ without pushing K⁺ out.
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Where does aldosterone actually do its work? In the aldosterone-sensitive distal nephron (ASDN): DCT2, CNT, and the collecting duct. The control room for Na⁺ balance and K⁺ homeostasis. (Follow the thread 🧵) #Nephpearls #Nephrology #Physiology
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8. Aldosterone: From Essential Tubular Regulator to Pathological Driver—Physiology, Disease, and Therapeutic Advances. In collaboration with @FrancescoPesce @DAmbrosioViola Open Access in @IJMS_MDPI: https://t.co/VLpwPTVvh8
mdpi.com
Aldosterone is a key regulator of sodium reabsorption, potassium secretion, and acid–base balance along the aldosterone-sensitive distal nephron (ASDN), where it exerts coordinated, segment-specific...
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7. Future & biomarkers 🔬 Non-genomic pathways (GPER), NLRP3 blockade, TLR/biglycan axis, miRNA, immune re-balancing and others. 👉The goal: pathway-informed, biomarker-guided precision nephrology.
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6. Therapies 💊 Steroidal MRAs: effective but hyperK + hormonal effects Non steroidal MRAs: Finerenone: anti-inflammatory/anti-fibrotic benefits w/ lower hyperK risk. Esaxerenone and Apararenone under investigation ASIs (baxdrostat/lorundrostat): source-targeting in the pipeline
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5. Primary vs secondary vs pseudo-hyperaldosteronism. 🧪Different renin/aldo signatures → different treatments.
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4. The aldosterone paradox 🤯 Co-signals (Ang II, K+) let the nephron dissociate Na⁺ retention from K⁺ secretion (NCC vs ENaC/ROMK). Context matters for therapy, electrolytes, and diuretics.
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3. MR ≠ aldosterone only. In tissues w/ low 11β-HSD2, cortisol activates MR → vascular dysfunction & fibrosis. 👉Blocking MR tackles pathology independent of BP.
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2. Low-salt world: survival. High-salt world: MR-driven inflammation, oxidative stress, albuminuria, CKD/CVD risk. 👉This ecological reframing explains why “normal” aldosterone can still harm. 🌿
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The success paradox: better therapies → rarer events → longer, costlier trials. Our proposal: smarter trials, not bigger, use adaptive & pragmatic designs, eGFR slope as surrogate, RWE and continue DHT monitoring. @FrancescoPesce
https://t.co/4V4HOTWBGS
mdpi.com
Clinical trials in nephrology have historically been hindered by significant challenges, including slow disease progression, patient heterogeneity, and recruitment difficulties. While recent therap...
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Proud to share our new paper: a road map to redesign nephrology clinical trials by pairing modern methodology and computational tools. With @FrancescoPesce. https://t.co/yld0y2d7JG
mdpi.com
Clinical trials in nephrology have historically been hindered by significant challenges, including slow disease progression, patient heterogeneity, and recruitment difficulties. While recent therap...
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Basics of Glomerulonephritis (GN). GBM is key. All patterns can be explained by glomerular basement membrane (GBM) & type of injury. Let’s do one at a time CRESCENTIC GN 1. Results from breach/break of GBM (red arrow) 2. Injury is sudden & severe Eg-ANCA & anti-GBM GN
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"Drink more water!" It's the easiest health advice around. Tired? Headache? Trying to be like Tom Brady? Just drink more water. But as a nephrologist, I get asked all the time: How much is the right amount? And the truth is... we don't really know. 🧵
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1/14 🤔 Why do we use iodine as an intravenous contrast agent? The answer requires a review of the composition of the human body and a brief tour of one of my favorites, the Periodic Table of Elements.
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🚨 Discover how intramolecular epitope spreading in PLA2R-associated Membranous Nephropathy escalates disease severity. As autoantibodies expand from CysR to CTLD domains, inflammation intensifies, driving proteinuria and reducing chances of remission. https://t.co/Ziz8J77tie
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